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Reshef, R.

Publications and source records attributed to Reshef, R..

5 recordsLinked to original sources

NMDA receptor-dependent Hebbian plasticity refines hippocampal spatial representations during two-dimensional navigation learning

Hippocampal place cell activity represents an animals location in space; yet, how hippocampal neuronal population dynamics change with spatial learning and the mechanisms underlying these activity changes, which drive allocentric navigation to a learned goal, are poorly understood. To address these questions, we performed calcium imaging with a novel wire-free waterproof miniaturized microscope to image the activity of large populations of hippocampal CA1 neurons during spatial learning of a two-dimensional navigational task, the Morris water maze. We followed the same cells during learning and were able to directly examine how each neuron in the ensemble, and the ensemble as a whole, changes its response properties. We found that neuronal spatial selectivity increased and population decoding of spatial location improved as mice learned to navigate to the goal. Viral CRISPR knock out of Grin1 (encoding the essential GluN1 NMDA receptor subunit) in dorsal hippocampal neurons, dramatically reduced long-term potentiation in CA1. This manipulation also prevented the increase in spatial selectivity and improvement of population decoding with spatial learning and resulted in learning deficits in the Morris water maze. Together, our results show that dorsal hippocampus NMDAR-dependent synaptic plasticity is essential for the learning-dependent refinement of CA1 place selectivity and improvement in population decoding of space.

neuroscience↗

A Donor T-Cell Receptor Structural Signature Determines Alloreactive Potential and Predicts Acute Graft-Versus-Host Disease

Acute graft-versus-host disease (GVHD) remains a lethal barrier to successful allogeneic hematopoietic cell transplantation, yet pre-transplant donor selection entirely ignores hypervariable T-cell receptor (TCR) architecture. Here, by characterizing over 64,000 alloreactive clonotypes, we demonstrate that human alloreactivity is dictated by a constrained, predictable baseline structural signature. Pathogenic, tissue-infiltrating alloreactive T cells exhibit significantly shortened CDR3{beta} regions, altered antigen-facing biophysical features, biased VJ gene usage and extensive inter-donor sharing originating from public anti-pathogen memory reservoirs. These potent clones natively cluster within the high-frequency fraction of the unstimulated baseline donor repertoire. We introduce R50, an assay-independent metric quantifying this clonal dominance, which independently predicted a six-fold increased risk of acute GVHD in a cross-institutional cohort. This scalable in silico platform shifts pre-transplant risk stratification from HLA typing and demographic surrogates to precision immune-receptor modeling.

immunology↗

Conserved Landscape of Chemokine Receptor Co-expression Defines the Functional States of CD8+ T Cells in Melanoma

Cancer immunotherapies, from checkpoint blockade to adoptive cell therapies like tumor-infiltrating lymphocytes (TILs), have revolutionized cancer treatment but are limited by variable efficacy and significant toxicities. A central challenge is identifying ideal T-cell populations that effectively eliminate tumors without causing off-target damage, a distinction not captured by existing biomarkers. We show that co-expression patterns of chemokine receptors (CRs) CXCR3, CCR5, and CXCR6 on CD8+ T cells provide a functional "code" defining subsets with divergent roles in on-target immunity versus off-target inflammation. In mouse and human melanoma, a triple-positive (CXCR3+CCR5+CXCR6+) T-cell subset is essential for tumor control, and its genetic signature correlates with positive clinical response, while a distinct CCR5+CXCR6+ subset drives liver immune-related adverse events (IRAEs). Crucially, this CR code reveals that immunotherapy actively reshapes T-cell trafficking patterns, uncovering profound heterogeneity within conventional populations and distinguishing potent anti-tumor progenitors from cells predisposed to exhaustion or off-target migration. This work establishes CR co-expression as a practical tool, providing a surface marker-based strategy to identify and enrich optimized T cells for adoptive therapies, thereby offering a framework to uncouple efficacy from toxicity. One Sentence SummaryCo-expression of CCR5, CXCR6, and CXCR3 provides a functional code that separates T-cell-mediated anti-tumor efficacy from off-target toxicity, enabling the selection of superior cells for safer and more effective cancer immunotherapies. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=120 SRC="FIGDIR/small/693486v2_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@19b0f44org.highwire.dtl.DTLVardef@1076129org.highwire.dtl.DTLVardef@17c0be6org.highwire.dtl.DTLVardef@f14893_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LI{middle dot} CXCR6, CXCR3 and CCR5 co-expression signature stratifies patient survival in human melanoma C_LIO_LI{middle dot} CD8+ T cells co-expressing CXCR6, CXCR3 and CCR5 are critical effectors with high proliferative, cytotoxic, and activation profile in human and mice melanoma C_LIO_LI{middle dot} CD8+ T cells co-expressing CXCR6, CXCR3 and CCR5 drive anti-tumoral responses during checkpoint blockade in both human and mice C_LI

immunology↗

Spatiotemporal Single-Cell Analysis Reveals T Cell Clonal Dynamics and Phenotypic Plasticity in Human Graft-versus-Host Disease

Allogeneic hematopoietic cell transplantation (alloHCT) is curative for various hematologic diseases but often leads to acute graft-versus-host disease (GVHD), a potentially life-threatening complication. We leverage GVHD as a uniquely tractable disease model to dissect complex T-cell-mediated pathology in 27 alloHCT recipients. We integrate pre-transplant identification of alloreactive T-cells with longitudinal tracking across blood and gut, using mixed lymphocyte reaction-based clonal "fingerprinting", TCR clonotyping, single-cell RNA/TCR sequencing, and spatial transcriptomics. Using DecompTCR, a novel computational tool for longitudinal TCR analysis, we uncover clonal expansion programs linked to GVHD severity and TCR features. Multi-omics profiling of gut biopsies reveals enrichment and clonal expansion of CD8 effector and ZNF683(Hobit) resident memory T-cells, cytolytic remodeling of regulatory and unconventional T-cells, and localization of CD8 effector T-cells near intestinal stem cells in crypt loss regions. This framework defines dynamic immune circuit rewiring and phenotypic plasticity with implications for biomarkers and therapies. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=198 SRC="FIGDIR/small/655962v1_ufig1.gif" ALT="Figure 1"> View larger version (45K): org.highwire.dtl.DTLVardef@178b77dorg.highwire.dtl.DTLVardef@569226org.highwire.dtl.DTLVardef@1951281org.highwire.dtl.DTLVardef@1f1e046_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIPersistent expansion of diverse alloreactive T cell clones is a hallmark of severe GVHD C_LIO_LIDecompTCR reveals dynamic clonal expansion programs linked to GVHD severity and clinical outcome C_LIO_LICD8+ T cell clones exhibit phenotypic plasticity in vivo across intestinal tissue compartments in GVHD C_LIO_LIHigh-resolution spatial profiling shows CD8+ effector T cells localize near intestinal stem cell niches and drive epithelial injury in GVHD C_LI

systems biology↗

Intratumoral CXCL12 Gradients Contextualize Tumor Cell Invasion, Migration and Immune Suppression in Breast Cancer

Although the CXCL12/CXCR4 pathway has been prior investigated for its prometastatic and immuno- suppressive roles in the tumor microenvironment, evidence on the spatiotemporal regulation of these hallmarks has been lacking. Here, we demonstrate that CXCL12 forms a gradient specifically around cancer cell intravasation doorways, also known as Tumor Microenvironment of Metastasis (TMEM) doorways, thus facilitating the chemotactic translocation of prometastatic tumor cells expressing CXCR4 toward the perivascular TMEM doorways for subsequent entry into peripheral circulation. Fur- thermore, we demonstrate that the CXCL12-rich micro-environment around TMEM doorways may cre- ate immunosuppressive niches, whereby CD8+ T cells, despite being attracted to these regions, often exhibit reduced effector functions, limiting their efficacy. While the CXCL12/CXCR4 pathway can mini- mally influence the overall composition of immune cell populations, it biases the distribution of CD8+ T cells away from TMEM doorways, justifying its prior-established role as immunosuppressive factor for CD8+ T cells. Our research suggests that the complex interactions between CXCL12 and the various tumor and immune cell types contributes not only to the completion of the initial steps of the metastatic cascade, but also offers an immunological "sanctuary" to prometastatic tumor cells homed around TMEM doorways. Overall, our study enhances our current understanding on the mechanisms, via which CXCL12 orchestrates tumor cell behavior and immune dynamics, potentially guiding future thera- peutic strategies to combat breast cancer metastasis and improve anti-tumor immunity.

cancer biology↗